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Death-associated protein kinase 3 (DAPK3) induces morphological changes in apoptosis when overexpressed in mammalian cells.
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For the first time, the present study showed that anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt (show AKT1 Antibodies) signaling pathway.
Activation of AKT (show AKT1 Antibodies) negatively regulates the pro-apoptotic function of DAPK3 in prostate cancer.
Methylation of DAPK3 at CpG1 but not CpG2 (show SYNE1 Antibodies) was lower in men with type 2 diabetes compared with healthy control men. Moreover, a glucose challenge was associated with lower CpG1 and CpG2 (show SYNE1 Antibodies) methylation in DAPK3 in both men with type 2 diabetes and healthy men.
DAPK3 controls proliferation, migration and tumor growth through activation of ERK (show EPHB2 Antibodies)/c-Myc (show MYC Antibodies) signaling in lung adenocarcinoma cells.
The results revealed mutations caused a significant structural variation in DAPK3, concentrated in flexible loops forming part of the ATP binding pocket which have been associated with very low kinase activity, and the cellular progression towards cancer
Cellular and mouse modeling studies show that DAPK3 is a tumor suppressor gene and is important in early development. Also, its expression is downregulated in more aggressive breast cancer relative to less aggressive and normal patient samples.
ROCK1 (show ROCK1 Antibodies) and ZIPK have diverse, but predominantly distinct regulatory functions in vascular SMC (show DYM Antibodies) and that ROCK1 (show ROCK1 Antibodies)-mediated activation of ZIPK is not involved in most of these functions.
DAPK3 plays a central role in preventing miR-17/miR (show MLXIP Antibodies)-20a depletion-induced genome instability and in miR-17/miR (show MLXIP Antibodies)-20a overexpression-triggered tumor formation.
These findings indicated that ZIPK may also be involved in the regulation of the cell cycle in human cells, by interacting with HsCdc14A.
findings suggest that ZIPK plays a role in the progression and completion of cytokinesis through MRLC phosphorylation
Cellular and mouse modeling studies show that DAPK3 is a tumor suppressor gene and is important in early development.
The C-terminal domain (NLS2 motif)of ZIPK of murine is nonfunctional for transport.
ZIPK may act as a cardiac RLC (show Dock5 Antibodies) kinase and thereby affect contractility.
murine ZIPK underwent specific divergence from a conserved consensus
Death-associated protein kinase 3 (DAPK3) induces morphological changes in apoptosis when overexpressed in mammalian cells. These results suggest that DAPK3 may play a role in the induction of apoptosis.
death-associated protein kinase 3
, Death-associated protein kinase 3
, death-associated protein kinase 3-like
, DAP kinase 3
, DAP-like kinase
, MYPT1 kinase
, ZIP kinase isoform
, zipper-interacting protein kinase
, ZIP kinase
, death-associated kinase 3
, Death-associated like kinase